ArticleNPJ precision oncology2024
Decoding gene regulatory circuitry underlying TNBC chemoresistance reveals biomarkers for therapy response and therapeutic targets.
Article in NPJ precision oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- The impact of intratumor heterogeneity on outcome and resistance to therapy in primary breast cancer: a systematic review.Medical oncology (Northwood, London, England) · 2026Pooled it
- Advances in Mechanism of Action and Efficacy of CBP/p300 Inhibitors in Different Subtypes of Breast Cancer.Molecules (Basel, Switzerland) · 2026Review
- Self-assembled verteporfin nanoparticles decrease drug efflux by P-glycoprotein without light activation in drug-resistant cancer cells.Bioengineering & translational medicine · 2026Article
- Tumor-infiltrating lymphocytes display prognostic signatures associated with chemotherapy response in TNBC patients.iScience · 2026Article
- DSTYK predicts Chemoresistance in Triple-Negative Breast Cancer Patient-Derived Xenograft Models.Research square · 2026Article
- Targeting Autophagy to Overcome Chemoresistance and Immune Resistance in Triple-Negative Breast Cancer.Cancers · 2026Review
- Spatial omics insights into tumor myeloid cells: roles in tumorigenesis, prognosis, and therapy.Molecular biology reports · 2026Review
- An Extracellular Matrix-Producing Subset of Cancer-Associated Fibroblasts Drives Chemoresistance in Breast Cancer via SRC Activation and G0S2 Upregulation.Cancer research · 2026Article
- Progress of siRNA Nanomedicines in Modulating the Microenvironment of Triple-Negative Breast Cancer.International journal of nanomedicine · 2026Review
- VASN Enhances IGF2BP3 Stability via USP10 Deubiquitination to Promote Triple-negative Breast Cancer Paclitaxel Resistance.International journal of biological sciences · 2026Article
- A single-cell network approach to decode metabolic regulation in gynecologic and breast cancers.NPJ systems biology and applications · 2025Article
- Short circuit: Transcription factor addiction as a growing vulnerability in cancer.Current opinion in structural biology · 2024Review
- Optimizing Antitumor Effect of Triple-Negative Breast Cancer via Rosmarinic Acid-β-Cyclodextrin Inclusion Complex.Pharmaceutics · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype characterised by extensive intratumoral heterogeneity, high rates of metastasis and chemoresistance, leading to poor clinical outcomes. Despite progress, the mechanistic basis of chemotherapy resistance in TNBC patients remains poorly understood. Here, leveraging single-cell transcriptome datasets of matched longitudinal TNBC chemoresponsive and chemoresistant patient cohorts, we unravel distinct cell subpopulations intricately associated with chemoresistance and the signature genes defining these populations. Notably, using genome-wide mapping of the H3K27ac mark, we show that the expression of these chemoresistance genes is driven via a set of TNBC super-enhancers and associated transcription factor networks across TNBC subtypes. Furthermore, genetic screens reveal that a subset of these transcription factors is essential for the survival of TNBC cells, and their loss increases sensitivity to chemotherapeutic agents. Overall, our study has revealed epigenetic and transcription factor networks underlying chemoresistance and suggests novel avenues to stratify and improve the treatment of patients with a high risk of developing resistance.
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.